Evidence map›Paper›PMID 16163384›Full record

ArticleThe EMBO journal2005

Novel role of p53 in maintaining mitochondrial genetic stability through interaction with DNA Pol gamma.

Geetha Achanta, Ryohei Sasaki, Li Feng, Jennifer S Carew, Weiqin Lu, Helene Pelicano, Michael J Keating, Peng Huang

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The EMBO journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

155 citing papers in PubMed, 2 syntheses or guidelines pooled it, 279 citations in OpenAlex.

  1. A systematic review of p53 regulation of oxidative stress in skeletal muscle.Redox report : communications in free radical research · 2018
    Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Mitochondrial Biogenesis in Skeletal Muscle.Advances in experimental medicine and biology · 2025
    Review
  9. Article
  10. Mitochondrial Reactive Oxygen Species (mROS) Generation and Cancer:International journal of nanomedicine · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

95 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Geetha AchantaDepartment of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Ryohei Sasaki
Li Feng
Jennifer S Carew
Weiqin Lu
Helene Pelicano
Michael J Keating
Peng Huang
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Superoxide, ROS, and novel targets for cancer therapyR01CA085563 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2001 to 2016
$3.1M
p53 in Cellular Response to ROS-Mediated DNA DamageR01CA100428 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2003 to 2012
$2.7M
Mitochondrial defects and Cancer TherapeuticsR01CA109041 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2004 to 2008
$1.6M
NCI NIH HHS CA100428NCI NIH HHS CA109041NCI NIH HHS CA16672NCI NIH HHS CA85563NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA085563NCI NIH HHS R01 CA100428NCI NIH HHS R01 CA109041
6 · The paper itself

Abstract

Mitochondrial DNA (mtDNA) mutations and deletions are frequently observed in cancer, and contribute to altered energy metabolism, increased reactive oxygen species (ROS), and attenuated apoptotic response to anticancer agents. The mechanisms by which cells maintain mitochondrial genomic integrity and the reason why cancer cells exhibit more frequent mtDNA mutations remain unclear. Here, we report that the tumor suppressor molecule p53 has a novel role in maintaining mitochondrial genetic stability through its ability to translocate to mitochondria and interact with mtDNA polymerase gamma (pol gamma) in response to mtDNA damage induced by exogenous and endogenous insults including ROS. The p53 protein physically interacts with mtDNA and pol gamma, and enhances the DNA replication function of pol gamma. Loss of p53 results in a significant increase in mtDNA vulnerability to damage, leading to increased frequency of in vivo mtDNA mutations, which are reversed by stable transfection of wild-type p53. This study provides a mechanistic explanation for the accelerating genetic instability and increased ROS stress in cancer cells associated with loss of p53.

Indexed as

Cell Line, TumorDNA DamageDNA-Directed DNA PolymeraseDNA, MitochondrialDNA Polymerase gammaDNA PrimersGenomic InstabilityHumansImmunoblottingImmunohistochemistryImmunoprecipitationMutationPolymerase Chain ReactionReactive Oxygen SpeciesTransfectionTumor Suppressor Protein p53DNA-Directed DNA PolymeraseDNA, MitochondrialDNA Polymerase gammaDNA PrimersReactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID16163384
PMCPMC1276176
OpenAlexW2128919887

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.